Interaction of acute and chronic stress with respiration: modification by naloxone.
Rats exposed to inescapable foot shock displayed an increase in respiratory rate, tidal volume and minute volume. Naloxone HCl (5 mg/kg, SC) potentiated the foot shock-induced increase in ventilation. Inhalation of high (5% and 10%) concentrations of carbon dioxide enhanced the stimulation of ventilation observed in both the acute stressed animals and the acute stress-naloxone treated group. Chronic daily foot shock sessions (11 days) attenuated the respiratory stimulation produced by acute foot shock and the potentiation induced by naloxone. The appearance of foot shock-induced stimulation of respiration paralleled the production of acute foot shock-induced analgesia. On the other hand, chronic foot shock attenuated both stress-related analgesia and respiratory stimulation. These results strongly suggest stress can influence respiratory function through activation or release of the endogenous opioids. It is postulated that the endorphinergic system functions as a compensatory system which prevents excessive stimulation of respiration by stress.
D000818:Animals; D002245:Carbon Dioxide / Q000097:blood; D004723:Endorphins / Q000502:physiology*; D008297:Male; D009270:Naloxone / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D012119:Respiration / Q000187:drug effects*; D013312:Stress, Physiological / Q000523:psychology*
D004723:Endorphins; D002245:Carbon Dioxide; D009270:Naloxone